Department of Medical Psychology and Neuropsychology, Center of Research on Psychology in Somatic diseases, Tilburg University, and Department of Cardiology, TweeSteden Hospital, Tilburg, The Netherlands.
J Affect Disord. 2012 Feb;136(3):567-76. doi: 10.1016/j.jad.2011.10.029. Epub 2011 Nov 30.
Little is known about whether cognitive/affective depressive symptoms or somatic/affective depressive symptoms are associated with inflammation in heart failure (HF), or that the relation is confounded with disease severity.
To examine the association between depressive symptom dimensions in HF patients with inflammatory markers cross-sectionally and prospectively, while adjusting for appropriate confounders.
Consecutive HF patients completed the Beck Depression Inventory at inclusion and at 12 month follow-up. Cytokines were assessed at both occasions. Cross-sectional--multivariate linear regression analysis (n=110) demonstrated that cognitive/affective depressive symptoms were independently associated with increased levels of sTNFR2 (β=0.20, p<0.05) and IL-1ra (β=0.28, p<0.01). Somatic/affective depressive symptoms were independently related to sTNFR2 (β=0.21, p<0.05). Prospective--(n=125) the level of cognitive/affective depressive symptoms at inclusion was prospectively associated with increased levels of sTNFR1 and sTNFR2 (β=0.21 and 0.25 resp. p<0.05), independent of covariates. Change in somatic/affective depressive symptoms over the 12 month period was associated with sTNFR2 (β=0.30, p=0.008). At symptom level, core depressive cognitions such as hopelessness and guilt drove the relation between the sTNF receptors and the cognitive/affective component, while having sleep problems was the most important associate of the somatic/affective dimension.
Baseline cognitive/affective depressive symptoms were prospectively associated with sTNFR1 and sTNFR2 in HF patients, while change in somatic/affective depressive symptoms was associated with sTNFR2, independent from clinical and demographic covariates. Further studies are warranted to replicate these findings and to examine the association between depression dimensions, inflammation and prognosis in HF.
关于认知/情感抑郁症状或躯体/情感抑郁症状是否与心力衰竭 (HF) 中的炎症有关，或者这种关系是否与疾病严重程度有关，目前知之甚少。
在调整适当的混杂因素后，横断面对 HF 患者抑郁症状维度与炎症标志物的关系进行前瞻性研究。
连续 HF 患者在纳入时和 12 个月随访时完成贝克抑郁量表。在两个时间点评估细胞因子。横断面——多元线性回归分析（n=110）表明，认知/情感抑郁症状与 sTNFR2 水平升高独立相关（β=0.20，p<0.05）和 IL-1ra（β=0.28，p<0.01）。躯体/情感抑郁症状与 sTNFR2 独立相关（β=0.21，p<0.05）。前瞻性-（n=125），纳入时认知/情感抑郁症状的水平与 sTNFR1 和 sTNFR2 水平升高呈前瞻性相关（β=0.21 和 0.25 分别为 p<0.05），独立于协变量。12 个月期间躯体/情感抑郁症状的变化与 sTNFR2 相关（β=0.30，p=0.008）。在症状水平上，无望和内疚等核心抑郁认知驱动了 sTNF 受体与认知/情感成分之间的关系，而睡眠问题是躯体/情感维度的最重要关联。
HF 患者基线认知/情感抑郁症状与 sTNFR1 和 sTNFR2 呈前瞻性相关，而躯体/情感抑郁症状的变化与 sTNFR2 相关，独立于临床和人口统计学协变量。需要进一步的研究来复制这些发现，并研究抑郁维度、炎症和 HF 预后之间的关系。
